This paper reports a versatile seed-mediated growth method for selectively synthesizing single-crystalline rhombic dodecahedral, octahedral, and cubic gold nanocrystals. In the seed-mediated growth method, cetylpyridinium chloride (CPC) and CPC-capped single-crystalline gold nanocrystals 41.3 nm in size are used as the surfactant and seeds, respectively. The CPC-capped gold seeds can avoid twinning during the growth process, which enables us to study the correlations between the growth conditions and the shapes of the gold nanocrystals. Surface-energy and kinetic considerations are taken into account to understand the formation mechanisms of the single-crystalline gold nanocrystals with varying shapes. CPC surfactants are found to alter the surface energies of gold facets in the order {100} > {110} > {111} under the growth conditions in this study, whereas the growth kinetics leads to the formation of thermodynamically less favored shapes that are not bounded by the most stable facets. The competition between AuCl(4)(-) reduction and the CPC capping process on the {111} and {110} facets of gold nanocrystals plays an important role in the formation of the rhombic dodecahedral (RD) and octahedral gold nanocrystals. Octahedral nanocrystals are formed when the capping of CPC on {111} facets dominates, while RD nanocrystals are formed when the reduction of AuCl(4)(-) on {111} facets dominates. Cubic gold nanocrystals are formed by the introduction of bromide ions in the presence of CPC. The cooperative work of cetylpyridinium and bromide ions can stabilize the gold {100} facet under the growth condition in this study, thereby leading to the formation of cubic gold nanocrystals.
The high-energy, high-intensity neutron fluxes produced by the fusion plasma will have a significant life-limiting impact on reactor components in both experimental and commercial fusion devices. As well as producing defects, the neutrons bombarding the materials initiate nuclear reactions, leading to transmutation of the elemental atoms. Products of many of these reactions are gases, particularly helium, which can cause swelling and embrittlement of materials. This paper integrates several different computational techniques to produce a comprehensive picture of the response of materials to neutron irradiation, enabling the assessment of structural integrity of components in a fusion power plant. Neutron-transport calculations for a model of the next-step fusion device DEMO reveal the variation in exposure conditions in different components of the vessel, while inventory calculations quantify the associated implications for transmutation and gas production. The helium production rates are then used, in conjunction with a simple model for He-induced grain-boundary embrittlement based on electronic-structure density functional theory calculations, to estimate the timescales for susceptibility to grain-boundary failure in different fusion-relevant materials. There is wide variation in the predicted grain-boundary-failure lifetimes as a function of both microstructure and chemical composition, with some conservative predictions indicating much less than the required lifetime for components in a fusion power plant.
In a fusion reactor materials will be subjected to significant fluxes of high-energy neutrons. As well as causing radiation damage, the neutrons also initiate nuclear reactions leading to changes in the chemical composition of materials (transmutation). Many of these reactions produce gases, particularly helium, which cause additional swelling and embrittlement of materials. This paper investigates, using a combination of neutron-transport and inventory calculations, the variation in displacements per atom (dpa) and helium production levels as a function of position within the high flux regions of a recent conceptual model for the 'next-step' fusion device DEMO. Subsequently, the gas production rates are used to provide revised estimates, based on new density-functional-theory results, for the critical component lifetimes associated with the helium-induced grain-boundary embrittlement of materials. The revised estimates give more optimistic projections for the lifetimes of materials in a fusion power plant compared to a previous study, while at the same time indicating that helium embrittlement remains one of the most significant factors controlling the structural integrity of fusion power plant components. * Corresponding author email: mark.gilbert@ccfe.ac.uk 1 lethargy interval is a commonly used measure for spectra of this type, and is equal to the natural logarithm of the ratio of a given energy-interval's upper bound to its lower bound.
Clear cell renal cell carcinoma (ccRCC) is the most aggressive RCC subtype with high metastasis, chemotherapy and radiotherapy resistance, and poor prognosis. This study attempted to establish the deregulations of miR-4521 and FAM129A together with their correlation to and mechanism of regulation of ccRCC development and progression. FAM129A acted as tumor promotor and miR-4521 acted as a suppressor in ccRCC. As measured in surgical tumorous tissues from ccRCC patients, FAM129A overexpression and miR-4521 deficiency together contributed to ccRCC progression by promoting advances in patients’ TNM stage and Fuhrman grade. Both the FAM129A knockdown and miR-4521 overexpression could reduce the in vitro migration and invasion abilities of renal cancer cells 786-O and ACHN, through the TIMP-1/MMP2/MMP9 pathway and could decrease their proliferation by promoting their apoptosis through the MDM2/p53/Bcl2/Bax pathway. By directly targeting the 3′-UTR domain of FAM129A , miR-4521 was negatively correlated with FAM129A /FAM129A levels in ccRCC progression and renal cancer cell malignancies. This work establishes the miR-4521-FAM129A axial regulation mechanism in ccRCC. Micro-4521 deficiency leads to FAM129A /FAM129A upregulation, which synergistically enhances the migration and invasion of renal cancer cells due to the induced decrease of TIMP-1 and increases of MMP2 and MMP9, and increases their growth through escaping apoptosis by suppressing p53 by way of upregulation of induced MDM2. The current work provides new clues to assist fundamental research into the diagnosis and treatment of ccRCC.
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